Measurements of neuron-specific and glia-specific proteins were used to characterize chemical-induced injury to the rat CNS. Trimethyltin (TMT), a neurotoxicant that preferentially damages neurons in limbic structures, was employed to produce consistent, time-dependent, dose- related, cell type-specific alterations in CNS morphology. Brain weights and histology were used to verify the cytopathological effects of TMT. Accompanying changes in 2 synaptic vesicle-associated proteins, synapsin I and p38, and the astrocyte-associated protein, glial fibrillary acidic protein (GFAP), were measured by radioimmunoassay (RIA). Immunohistochemistry of GFAP and incorporation of 3H-thymidine into GFAP-positive astrocytes also were used to characterize astrocytic responses to TMT-induced injury. Finally, quantitative 2-dimensional PAGE was employed to detect additional proteins affected by TMT. Acute administration of TMT caused large dose- and time-dependent decreases in synapsin I and p38 in hippocampus; the same proteins were largely unaffected in a nonlimbic structure, the frontal cortex. Twelve weeks after dosing, the concentrations of synapsin I and p38 and, to a lesser extent, the absolute amount of these proteins in hippocampus had returned to near control values, findings that are suggestive of reactive synaptogenesis. TMT caused large dose- and time-dependent increases in GFAP that were not confined to hippocampus. Twelve weeks after dosing, the amounts of GFAP in hippocampus and frontal cortex had returned to near control values, findings indicative of a transient astrocytic response to brain injury. Immunohistochemistry of GFAP revealed widespread astrocytic reactivity as a consequence of exposure to TMT, a response that resulted in part from the proliferation of astrocytes. Additional neurotypic proteins altered by TMT-induced injury included one of the neurofilament (NF) triplet proteins (p68) and a protein with the electrophoretic characteristics of neuron- specific enolase (NSE). The data indicate that measurements of neurotypic and gliotypic proteins may be used to characterize the temporal and regional patterns of neuronal and glial responses to injury.

https://www.jneurosci.org/content/jneuro/7/4/931.full.pdf

Quantitative changes in the synaptic vesicle proteins synapsin I and p38 and the astrocyte-specific protein glial fibrillary acidic protein are associated with chemical-induced injury to the rat central nervous system.

The pharmacological treatment of subjects who sustain a brain lesion, either accidentally (trauma, stroke) or surgically (tumor excision, stereotactic lesions, etc.) is generally aimed at preventing further damage from pathology such as edema, hemorrhage, infection. seizures, or renal or cardiopulmonary failure. The efficacy of these treatments can be observed in the period immediately following the insult. However, the long-term effects, if any, of these treatments, or any interactions between the drugs used and mechanisms involved in functional recovery, have often been ignored. A brief review of some basic aspects of the response of neural and nonneural cells to injury is offered, with some comments on events occurring during histogenesis and in the initiation and regulation of inflammatory and immune responses that might be relevant to the problem of brain plasticity. I then discuss some of the mechanisms of cell damage common to different forms of injury (e.g., trauma, hemorrhage, thrombosis) such as membrane permeability changes, intracellular calcium alterations, and the role of certain neurotransmitters in the genesis of acute neuronal loss. Special emphasis on ischemia is made, with a review of the pharmacological treatment of stroke and comments on the importance of the management of the medical and neurological complications of a brain lesion. I conclude with a discussion of the requirements in the design of clinical trials oriented towards the individualization of drug therapy. Finally, I summarize our own investigations with a pharmacological model of reversible brain dysfunction using GABA, an endogenous inhibitory neurotransmitter, in both rats and monkeys.

Pharmacological Approaches to the Treatment of Brain and Spinal Cord Injury

The recent surge of interest in cytoskeletal 10-nm filaments is attributable to the discovery of the cell specificity of their protein subunits. In immature skeletal muscle, 10-nm filaments were first called “intermediate” because their diameter was between that of thin actin and thick myosin filaments (Ishikawa et al., 1968). The term is now applied to all 10-nm filaments regardless of their location. In nonmuscle cells, “intermediate” stands for a diameter between that of actin microfilaments and microtubules.

Intermediate filaments in nervous tissue.

Wallerian degeneration: history and clinical significance.

https://dspace.library.uu.nl/bitstream/handle/1874/3757/schotman_84_evidence%20that%20the%20neurotrophic%20actions.pdf;sequence=2

Evidence that the neurotrophic actions of α-MSH may derive from its ability to mimick the actions of a peptide formed in degenerating nerve stumps

To identify axonal proteins which are unique constituents of neurons, the spectrum of detectable proteins of degenerating nerves has been compared with that of intact control nerves from the same animals. Wallerian degeneration was induced in rabbits by unilateral transection of the optic and sciatic nerves. Proteins of nerve homogenates were compared by sodium dodecyl sulfate-gel electrophoresis and by two- dimensional electrophoresis. Four non-myelin proteins disappear from degenerating nerve. These include the three neurofilament proteins (P68, P150, and P200) and a polypeptide with a molecular weight of about 65,000 daltons (P65) which is not associated with filaments.

https://www.jneurosci.org/content/jneuro/1/5/461.full.pdf

The loss of neuron-specific proteins during the course of Wallerian degeneration of optic and sciatic nerve

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The loss of neuron-specific proteins during the course of Wallerian degeneration of optic and sciatic nerve